Differential functions of G protein and Baz-aPKC signaling pathways in Drosophila neuroblast asymmetric division

Yasushi Izumi, Nao Ohta, Asako Itoh-Furuya, Naoyuki Fuse, Fumio Matsuzaki

研究成果: Article査読

86 被引用数 (Scopus)

抄録

Drosophila melanogaster neuroblasts (NBs) undergo asymmetric divisions during which cell-fate determinants localize asymmetrically, mitotic spindles orient along the apical-basal axis, and unequal-sized daughter cells appear. We identified here the first Drosophila mutant in the Gγ1 subunit of heterotrimeric G protein, which produces Gγ1 lacking its membrane anchor site and exhibits phenotypes identical to those of Gβ13F, including abnormal spindle asymmetry and spindle orientation in NB divisions. This mutant fails to bind Gβ13F to the membrane, indicating an essential role of cortical Gγ1-Gβ13F signaling in asymmetric divisions. In Gγ1 and Gβ13F mutant NBs, Pins-Gαi, which normally localize in the apical cortex, no longer distribute asymmetrically. However, the other apical components, Bazooka-atypical PKC-Par6-Inscureable, still remain polarized and responsible for asymmetric Miranda localization, suggesting their dominant role in localizing cell-fate determinants. Further analysis of Gβγ and other mutants indicates a predominant role of Partner of Inscureable-Gαi in spindle orientation. We thus suggest that the two apical signaling pathways have overlapping but different roles in asymmetric NB division.

本文言語English
ページ(範囲)729-738
ページ数10
ジャーナルJournal of Cell Biology
164
5
DOI
出版ステータスPublished - 2004 3月 1
外部発表はい

ASJC Scopus subject areas

  • 細胞生物学

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